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Updated: Jan 28, 2026

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Published on: December 28, 2021
The activity of transient receptor potential channel C-6 modulates the differentiation of fat cells
Yan Qin Tan1, Hiu Yee Kwan2, Xiaoqiang Yao3
1School of Life Sciences, Faculty of Science, The Chinese University of Hong Kong, Hong Kong, China.
Abstract:
Previously, the V1-3 isoforms of the transient receptor potential channel (TRP) have been shown to promote or prevent adipocyte differentiation. In the current study, the C isoforms were screened for blocking adipogenesis. The hypothesis that the TRP classic or canonical (TRPC) deters adipocyte differentiation was investigated in 3T3-L1 cells employing the channel-specific activator and antagonist, silencing, and overexpression techniques. Fat accumulation in cells was visualized by Oil Red O staining. Intracellular calcium inflow was estimated by confocal microscopy. A high-fat (HF) feeding study was also performed on C57BL/6J mice to verify the findings in the cell model. Among the 6 C isoforms tested, only TRPC-6 inhibited the differentiation of fat cells. The phytochemical quercetin induced the channel protein expression. Calcium-imaging results also revealed that the flavonoid could trigger calcium inflow. Coadministration of quercetin (1 or 20 mg/kg body weight) in an HF diet prevented TRPC-6 from declining and attenuated phosphorylated (p)-PKB and PI3k, as well as the proliferation of visceral fat cells. The present study illustrated that TRPC-6 activation could perturb adipocyte differentiation. The food flavonoid quercetin was a TRPC-6 inducer and activator and it could prevent adipogenesis in mice.-Tan, Y. Q., Kwan, H. Y., Yao, X., Leung, L. K. The activity of transient receptor potential channel C-6 modulates the differentiation of fat cells.
Insights
Transient Receptor Potential Canonical (TRPC)-6 inhibits fat cell differentiation. The flavonoid quercetin activates TRPC-6, preventing adipogenesis in mice fed a high-fat diet.
Area of Science:
- Cell Biology
- Physiology
- Biochemistry
Background:
- Previous studies linked TRP V1-3 isoforms to adipocyte differentiation.
- The role of TRP C isoforms in adipogenesis remained largely unexplored.
Purpose of the Study:
- To investigate the role of TRP C isoforms in adipocyte differentiation.
- To determine if TRPC-6 activation inhibits adipogenesis and if quercetin modulates this process.
Main Methods:
- Screening of 6 TRPC isoforms for adipogenesis inhibition in 3T3-L1 cells.
- Utilized channel activators, antagonists, silencing, and overexpression techniques.
- Assessed fat accumulation via Oil Red O staining and intracellular calcium via confocal microscopy.
- Conducted a high-fat diet study in C57BL/6J mice.
Main Results:
- TRPC-6 was identified as the sole TRPC isoform inhibiting fat cell differentiation.
- The phytochemical quercetin induced TRPC-6 expression and calcium influx.
- Quercetin administration in high-fat diet-fed mice prevented TRPC-6 decline and attenuated p-PKB and PI3k signaling.
- Quercetin also reduced visceral fat cell proliferation.
Conclusions:
- TRPC-6 activation significantly perturbs adipocyte differentiation.
- The dietary flavonoid quercetin acts as a TRPC-6 inducer and activator, inhibiting adipogenesis in vivo.
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